Notch-2 is a 300 kDa type I transmembrane glycoprotein that is one of four human Notch homologues involved in developmental processes. Functions as a receptor for membrane-bound ligands Jagged-1 (JAG1), Jagged-2 (JAG2) and Delta-1 (DLL1) to regulate cell-fate determination. Human Notch-2 ECD (aa 26-530) shows 93%, 93%, 96% and 96% aa identity with the corresponding regions of mouse, rat, canine, and bovine Notch-2, respectively. Hajdu Cheney Syndrome (HCS) is a rare disease associated with mutations of NOTCH2 that lead to the translation of a truncated, presumably stable, NOTCH2 protein. NOTCH2 is down-regulated in colon cancer, and reduced expression is associated with a less differentiated, more aggressive phenotype, and reduced overall survival. NOTCH2 has also been shown to have pro-apoptotic and growth suppressive effects in thyroid carcinoma, and carcinoid tumors. NOTCH2 acts as an oncogene that promotes bladder cancer growth and metastasis through EMT, cell-cycle progression, and maintenance of stemness.
Human Notch-3 is part of the Notch family of type I transmembrane glycoproteins involved in a number of early-event developmental processes . The extracellular domain of Notch receptors interact with the extracellular domain of transmembrane ligands Jagged, Delta, and Serrate expressed on the surface of a neighboring cell. In both vertebrates and invertebrates, Notch signaling is important for specifying cell fates and for defining boundaries between different cell types.
NADPH Oxidase 4/NOX4, also known as Renal NADPH Oxidase/RENOX and Kidney Oxidase 1/KOX1, is a 66 to 75 kDa member of the NOX family of NADPH oxidases. NOX family members are a major source of reactive oxygen species (ROS), including hydrogen peroxide and superoxide, and are critical mediators of redox signaling. NOX4 is strongly expressed in the kidney, especially in the proximal convoluted tubule cells of the renal cortex, and may function as an oxygen sensor that regulates the synthesis of erythropoietin. Expression is also high in endothelial cells, and because aortas from deficient mice exhibit increased inflammation, hypertrophy and endothelial dysfunction, NOX4 may function to protect the vasculature during ischemic or inflammatory stress. Human NOX4 is 578 amino acids (aa) in length, with several additional smaller isoforms identified. Over aa 450-578, human NOX4 has 92% sequence identity with mouse NOX4, and 91% identity with rat NOX4.
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